2020-06-06T03:43:06Z http://digital.csic.es/dspace-oai/request
oai:digital.csic.es:10261/182221 2019-05-24T00:58:35Z com_10261_11773 com_10261_1 col_10261_11778
Regulation of Platelet Function by Orai, STIM and TRP Berna-Erro, Alejandro Jardín, Isaac Smani, Tarik Rosado, Juan A. Ministerio de Economía y Competitividad (España) European Commission Junta de Extremadura Orai1 TRPC1 STIM1 Calcium entry Human platelets TRPC6 Rosado J. (eds). Agonist-induced changes in cytosolic Ca2+ concentration ([Ca2+]c) are central events in platelet physiology. A major mechanism supporting agonist-induced Ca2+ signals is store-operated Ca2+ entry (SOCE), where the Ca2+ sensor STIM1 and the channels of the Orai family, as well as TRPC members are the key elements. STIM1-dependent SOCE plays a major role in collagen-stimulated Ca2+ signaling, phosphatidylserine exposure and thrombin generation. Furthermore, studies involving Orai1 gain-of-function mutants and platelets from Orai1-deficient mice have revealed the importance of this channel in thrombosis and hemostasis to those found in STIM1-deficient mice indicating that SOCE might play a prominent role in thrombus formation. Moreover, increase in TRPC6 expression might lead to thrombosis in humans. The role of STIM1, Orai1 and TRPCs, and thus SOCE, in thrombus formation, suggests that therapies directed against SOCE and targeting these molecules during cardiovascular and cerebrovascular events could significantly improve traditional anti-thrombotic treatments. 2019-05-23T13:43:50Z 2019-05-23T13:43:50Z 2016 comunicación de congreso Calcium Entry Pathways in Non-excitable Cells: 157-181 (2016) 978-3-319-26972-6 0065-2598 http://hdl.handle.net/10261/182221 10.1007/978-3-319-26974-0_8 http://dx.doi.org/10.13039/501100000780 http://dx.doi.org/10.13039/501100003329 eng Advances in Experimental Medicine and Biology 898 https://doi.org/10.1007/978-3-319-26974-0_8 MINECO/ICTI2013-2016/BFU2013-45564-C2-1-P MINECO/ICTI2013-2016/BFU2013-45564-C2-2-P closedAccess Springer Nature